Three independent lines of investigation in normal man suggest that circulating and intrarenal angiotensin II levels represent a major determinant of resting renal blood flow and the major determinant of the renal vascular response to angiotensin II. Thus a reduction in sodium intake, a reduction in potassium intake, or the ingestion of oral contraceptive agents on any diet, all result in an increase in the circulating levels of renin, angiotension II, and a reduction in renal blood flow as well as a reduced response to angiotensin II infused into the renal artery. Conversely, essential hypertension is associated with a potentiated response to angiotensin II: it is thus unlikely that intrarenal angiotensin II plays a role in the increase in renal vascular resistance in patients with "normal-renin" hypertension. In patients with essential hypertension, several lines of evidence suggest an increase in vascular tone. There is an increase in moment-to-moment variability; enhanced response to nonspecific vasodilator such as acetylcholine and dopamine; and a blood flow increase induced by phentolamine, an alpha adrenergic blocking agent. Phentolamine does not increse renal blood flow in normal man. All of the vasodilators also reverse, in part or in toto, the angiographic abnormalities associated with the blood flow reduction. Measurements with dopamine-beta-hydroxylase in arterial and renal vein plasma demonstrate a significant increase in patients with essential hypertension. Thus several lines of evidence suggest that in many patients with essential hypertension the increase in renal vascular resistance is functional, due to active vasoconstriction, perhaps mediated by the sympathetic nervous system.